Evidence map›Paper›PMID 26716649›Full record

ArticleOncotarget2016

Simultaneous gene silencing of KRAS and anti-apoptotic genes as a multitarget therapy.

Kristin Werner, Franziska Lademann, May-Linn Thepkaysone, Beatrix Jahnke, Daniela E Aust, Christoph Kahlert, Georg Weber, Jürgen Weitz, Robert Grützmann, Christian Pilarsky

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 15 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Kristin WernerDepartment of Visceral, Thoracic and Vascular Surgery, TU Dresden, 01307 Dresden, Germany.
Franziska LademannDepartment of Visceral, Thoracic and Vascular Surgery, TU Dresden, 01307 Dresden, Germany.
May-Linn ThepkaysoneDepartment of Visceral, Thoracic and Vascular Surgery, TU Dresden, 01307 Dresden, Germany.
Beatrix JahnkeDepartment of Visceral, Thoracic and Vascular Surgery, TU Dresden, 01307 Dresden, Germany.
Daniela E AustInstitute of Pathology, TU Dresden, 01307 Dresden, Germany.
Christoph KahlertDepartment of Visceral, Thoracic and Vascular Surgery, TU Dresden, 01307 Dresden, Germany.
Georg WeberDepartment of Surgery, Universitätsklinikum Erlangen, 91054 Erlangen, Germany.
Jürgen WeitzDepartment of Visceral, Thoracic and Vascular Surgery, TU Dresden, 01307 Dresden, Germany.
Robert GrützmannDepartment of Surgery, Universitätsklinikum Erlangen, 91054 Erlangen, Germany.
Christian PilarskyDepartment of Visceral, Thoracic and Vascular Surgery, TU Dresden, 01307 Dresden, Germany.
TU Dresden · DEUniversitätsklinikum Erlangen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer is one of the most lethal tumor types worldwide and an effective therapy is still elusive. Targeted therapy focused against a specific alteration is by definition unable to attack broad pathway signaling modification. Tumor heterogeneity will render targeted therapies ineffective based on the regrowth of cancer cell sub-clones. Therefore multimodal therapy strategies, targeting signaling pathways simultaneously should improve treatment.SiRNAs against KRAS and the apoptosis associated genes BCLXL, FLIP, MCL1L, SURVIVIN and XIAP were transfected into human and murine pancreatic cancer cell lines. Induction of apoptosis was measured by Caspase 3/7 activation, subG1 FACS analysis and PARP cleavage. The therapeutic approach was tested in a subcutaneous allograft model with a murine cancer cell line.By using siRNAs as a systematic approach to remodel signal transduction in pancreatic cancer the results showed increasing inhibition of proliferation and apoptosis induction in vitro and in vivo. Thus, siRNAs are suitable to model multimodal therapy against signaling pathways in pancreatic cancer. Improvements in in vivo delivery of siRNAs against a multitude of targets might therefore be a potential therapeutic approach.

Indexed as

Gene SilencingAdaptor Proteins, Signal TransducingAnimalsApoptosisbcl-X ProteinBlotting, WesternCell ProliferationFemaleHumansInhibitor of Apoptosis ProteinsMiceMyeloid Cell Leukemia Sequence 1 ProteinPancreatic NeoplasmsProto-Oncogene Proteins p21(ras)Real-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionAdaptor Proteins, Signal TransducingBCL2L1 protein, humanbcl-X ProteinBIRC5 protein, humanInhibitor of Apoptosis ProteinsKRAS protein, humanMCL1 protein, humanMyeloid Cell Leukemia Sequence 1 ProteinProto-Oncogene Proteins p21(ras)RNA, MessengerRNA, Small InterferingSurvivinTNIP2 protein, humanXIAP protein, humanX-Linked Inhibitor of Apoptosis ProteinapoptosisKRASpancreatic cancerRNAisimultaneous gene silencing

Identifiers

PMID26716649
PMCPMC4826184
OpenAlexW2212465418

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.